ABSTRACr'. The ductus venosus allows highly oxygenated blood returning from the umbilical-placental circulation to bypass the liver, and is believed thereby to facilitate preferential distribution of this blood to the fetal brain and heart. To examine this hypothesis, we developed a model that allows acute obstruction of the ductus venosus in chronically catheterized fetal lambs. In seven fetal lambs, a Swann-Ganz catheter was inserted into the inferior vena cava and the balloon tip advanced into the ductus venosus. Control measurements were obtained 1-2 d after surgery, before and during inflation of the balloon in the ductus venosus. At each sample time, radioactive microspheres were injected to determine organ blood flow and the distribution of umbilical venous blood flow. During balloon inflation, the percentage of umbilical venous return passing through the ductus venosus was reduced from 38 2 15% to 1 f 0.5%. Umbilical-placental blood flow was unchanged from control values of 181 f 33 mL/min/kg. Total liver blood flow increased from 346 f 98 to 553 f 105 mL/min/ 100 g. Pressure in the inferior vena cava did not change, but umbilical venous pressure increased from 7.2 2 2.7 to 8.7 f 3.5 mm Hg. Total vascular resistance across the liver and ductus venosus increased from 0.013 ? 0.006 to 0.020 2 0.011 during ductus venosus obstruction. Fetal heart rate, arterial blood pressure, and descending aortic pH and blood gases were unchanged, as was oxygen content in the descending aorta and carotid artery. Organ blood flows, combined ventricular output, and oxygen delivery were also unchanged. In five animals, these studies were repeated during maternal hypoxemia. Similar changes in liver blood flow were observed. Organ blood flows and oxygen delivery were not altered by ductus venosus obstruction during hypoxemia. We conclude that obstruction of the ductus venosus has no effect on regional blood flow distribution or oxygen delivery in normoxemic or hypoxemic animals. Because the hepatic microcirculation has such a high compliance, the ductus venosus is not crucial in regulating umbilical venous return to the central fetal circulation. (Pediatr Res 29: 347-352, 1991) Up to 50% of the blood returning from the umbilical-placental circulation passes through the ductus venosus in the fetal lamb. The rest of the blood passes through the hepatic sinusoids and then drains into the inferior vena cava. Streaming patterns in the inferior vena cava and right atrium preferentially distribute the highly oxygenated blood that passes through the ductus venosus to the fetal brain and heart (1). During umbilical cord compression (2) and fetal hemorrhage (3), increasing proportions of the blood returning in the umbilical vein from the placenta pass through the ductus venosus. These observations have suggested that the ductus venosus facilitates the preferential distribution of highly oxygenated blood to the fetal brain and heart. However, the role of the ductus venosus is uncertain. The fetal foal, swine, and guinea pig lack a duct...

No abstract

No abstract

Acute fetal hypoxemia increases the vascular resistance of the umbilical veins as well as that of the liver. Because, at least in the human, the umbilical-placental circulation has no autonomic innervation, circulating hormones could well be responsible for this increase in umbilical-placental outflow resistance. In chronically instrumented fetal sheep, norepinephrine, epinephrine, vasopressin, and angiotensin II were infused in sequentially increasing doses into the descending aorta and vascular resistance to umbilical-placental blood flow was measured. Norepinephrine and epinephrine increased the vascular resistance of the umbilical veins in a dose-dependent manner. Both catecholamines also increased the vascular resistance of the liver, resulting in an increase in ductus venosus blood flow. In contrast, vasopressin and angiotensin II had no effect on umbilical-placental outflow resistance. Thus catecholamines may be responsible for the increase in the vascular resistance of the umbilical veins and liver in response to acute fetal hypoxemia.

It has been suggested that the umbilical-placental circulation is maximally vasodilated under normal conditions. To test this hypothesis, we investigated the effect of vasodilators on umbilical-placental vascular resistance. In nine chronically instrumented fetal lambs, catheters were placed in the descending aorta, umbilical artery, umbilical vein, and inferior vena cava. Umbilical-placental blood flow was measured by an electromagnetic flow probe placed around the common umbilical artery. Forskolin and nitroglycerin both dilated the umbilical-placental circulation, causing a dose-dependent decrease in umbilical-placental resistance to approximately 80% of baseline, indicating that the umbilical-placental circulation has some dilatory reserve. Both the adenosine 3',5'-cyclic monophosphate and the guanosine 3',5'-cyclic monophosphate mechanisms, which are directly stimulated by forskolin and nitroglycerin, respectively, are functional in the umbilical-placental circulation. However, the vasodilators prostacyclin and adenosine, which act through specific cell membrane receptors, have no effect on the umbilical-placental resistance. The inability of these agents to dilate the umbilical-placental circulation could be due to a lack of the appropriate receptors in the umbilical-placental vasculature.